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Open Access Highly Accessed Research article

Decreased brain venous vasculature visibility on susceptibility-weighted imaging venography in patients with multiple sclerosis is related to chronic cerebrospinal venous insufficiency

Robert Zivadinov12*, Guy U Poloni1, Karen Marr1, Claudiu V Schirda1, Christopher R Magnano1, Ellen Carl1, Niels Bergsland1, David Hojnacki2, Cheryl Kennedy1, Clive B Beggs3, Michael G Dwyer1 and Bianca Weinstock-Guttman2

Author Affiliations

1 Buffalo Neuroimaging Analysis Center, University at Buffalo, Buffalo, NY, USA

2 The Jacobs Neurological Institute, University at Buffalo, Buffalo, NY, USA

3 Centre for Infection Control and Biophysics, University of Bradford, Bradford, UK

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BMC Neurology 2011, 11:128  doi:10.1186/1471-2377-11-128

Published: 19 October 2011

Abstract

Background

The potential pathogenesis between the presence and severity of chronic cerebrospinal venous insufficiency (CCSVI) and its relation to clinical and imaging outcomes in brain parenchyma of multiple sclerosis (MS) patients has not yet been elucidated. The aim of the study was to investigate the relationship between CCSVI, and altered brain parenchyma venous vasculature visibility (VVV) on susceptibility-weighted imaging (SWI) in patients with MS and in sex- and age-matched healthy controls (HC).

Methods

59 MS patients, 41 relapsing-remitting and 18 secondary-progressive, and 33 HC were imaged on a 3T GE scanner using pre- and post-contrast SWI venography. The presence and severity of CCSVI was determined using extra-cranial and trans-cranial Doppler criteria. Apparent total venous volume (ATVV), venous intracranial fraction (VIF) and average distance-from-vein (DFV) were calculated for various vein mean diameter categories: < .3 mm, .3-.6 mm, .6-.9 mm and > .9 mm.

Results

CCSVI criteria were fulfilled in 79.7% of MS patients and 18.2% of HC (p < .0001). Patients with MS showed decreased overall ATVV, ATVV of veins with a diameter < .3 mm, and increased DFV compared to HC (all p < .0001). Subjects diagnosed with CCSVI had significantly increased DFV (p < .0001), decreased overall ATVV and ATVV of veins with a diameter < .3 mm (p < .003) compared to subjects without CCSVI. The severity of CCSVI was significantly related to decreased VVV in MS (p < .0001) on pre- and post-contrast SWI, but not in HC.

Conclusions

MS patients with higher number of venous stenoses, indicative of CCSVI severity, showed significantly decreased venous vasculature in the brain parenchyma. The pathogenesis of these findings has to be further investigated, but they suggest that reduced metabolism and morphological changes of venous vasculature may be taking place in patients with MS.